Elucidating the role of circNFIB in myocardial fibrosis alleviation by endogenous sulfur dioxide.

BACKGROUND: To investigate the role of circNFIB in the alleviation of myocardial fibrosis by endogenous sulfur dioxide (SO2). METHODS: We stimulated cultured neonatal rat cardiac fibroblasts with transforming growth factor-ß1 (TGF-ß1) and developed an in vitro myocardial fibrosis model. Lentivirus vectors containing aspartate aminotransferase 1 (AAT1) cDNA were used to overexpress AAT1, and siRNA was used to silence circNFIB. The SO2, collagen, circNFIB, Wnt/ß-catenin, and p38 MAPK pathways were examined in each group. RESULTS: In the in vitro TGF-ß1-induced myocardial fibrosis model, endogenous SO2/AAT1 expression was significantly decreased, and collagen levels in the cell supernatant and type I and III collagen expression, as well as α-SMA expression, were all significantly increased. TGF-ß1 also significantly reduced circNFIB expression. AAT1 overexpression significantly reduced myocardial fibrosis while significantly increasing circNFIB expression. Endogenous SO2 alleviated myocardial fibrosis after circNFIB expression was blocked. We discovered that circNFIB plays an important role in the alleviation of myocardial fibrosis by endogenous SO2 by inhibiting the Wnt/ß-catenin and p38 MAPK pathways. CONCLUSION: Endogenous SO2 promotes circNFIB expression, which inhibits the Wnt/ß-catenin and p38 MAPK signaling pathways, consequently alleviating myocardial fibrosis.

Microplastics in take-out food: Are we over taking it?

Take-out food has become increasingly prevalent due to the fast pace of people's life. However, few study has been done on microplastics in take-out food. Contacting with disposable plastic containers, take-out food may be contaminated with microplastics. In the present study, abundance and characteristics of microplastics in total of 146 take-out food samples including solid food samples and beverage samples (bubble tea and coffee) were determined and identified. The mean abundance of microplastics in take-out food was 639 items kg-1, with the highest value in rice and the lowest value in coffee. Fragments shape, transparent color and sizes ≤ 500 µm were the main characteristics of microplastics in those food, and polyethylene was the main polymer type. Our results indicated that microplastics in take-out food was influenced by food categories and cooking methods, as well as food packaging materials. Approximately 170-638 items of microplastics may be consumed by people who order take-out food 1-2 times weekly.

JNK pathway-associated phosphatase illustrates low expression and negative correlations with inflammation, disease activity, and T-helper 17 cells in inflammatory bowel disease children.

BACKGROUND: C-Jun N-terminal kinase pathway-associated phosphatase (JKAP) modulates the T cell receptor and mitogen-activated protein kinase pathway-mediated autoimmunity, thus participating in the pathogenesis of autoimmune diseases. This study aimed to explore the clinical implication of JKAP in inflammatory bowel disease (IBD) children. METHODS: C-Jun N-terminal kinase pathway-associated phosphatase, tumor necrosis factor-α (TNF-α), interleukin-23, interferon-γ (T-helper 1 secreted cytokine), and interleukin-17A (T-helper 17 secreted cytokine) in serum samples from 140 IBD children (including 60 Crohn's disease (CD) children and 80 ulcerative colitis (UC) children) were detected by ELISA. Meanwhile, JKAP from serum samples of 10 healthy controls (HCs) was also detected by ELISA. RESULTS: C-Jun N-terminal kinase pathway-associated phosphatase was reduced in CD children (median (interquartile range (IQR)): 51.6 (36.8-69.5) pg/ml) and UC children (median (IQR): 57.5 (43.4-78.5) pg/ml) compared with HCs (median (IQR): 101.8 (70.0-143.2) pg/ml) (both p < 0.05). In CD children, JKAP was negatively correlated with C-reactive protein (CRP) (p = 0.016) and erythrocyte sedimentation rate (ESR) (p = 0.029); while in UC children, JKAP was also negatively correlated with CRP (p = 0.006) and ESR (p = 0.022). Regarding the correlation of JKAP with disease activity, it presented negative correlations with PCDAI (p = 0.001) and PUCAI (p = 0.002). Besides, JKAP was negatively related to TNF-α (both p < 0.05) but not interleukin-23 (both p>0.05) in CD and UC children. Additionally, JKAP was not correlated with interferon-γ in CD or UC children (both p>0.05), while negatively correlated with interleukin-17A in CD and UC children (both p < 0.05). CONCLUSION: C-Jun N-terminal kinase pathway-associated phosphatase shows low expression and negative correlations with inflammation, disease activity, and T-helper 17 cells in IBD children.

Serum dual-specificity phosphatase 1 reflects decreased exacerbation risk, correlates with less advanced exacerbation severity and lower inflammatory cytokines in children with asthma.

BACKGROUND: It is as fact that dual-specificity phosphatase 1 (DUSP1) regulates the T cell activation, pro-allergic response, and inflammation to engage with the pathogenesis of asthma, but its clinical role in children with asthma is unclear. The present study aimed to explore the expression of DUSP1, its association with exacerbation risk, severity, and inflammatory cytokines in children with asthma. METHOD: Around 52 children with asthma-exacerbation, 50 children in asthma-remission, and 50 healthy children were chosen for the study. The serum levels of DUSP1, as well as tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, and IL-17 were detected by the enzyme-linked immunosorbent assay. RESULTS: The levels of DUSP1 was the highest in healthy children (median (IQR)=34.305 (25.892- 43.693) ng/mL), the second highest in children in asthma-remission (median (IQR)=21.471 (18.581-27.934) ng/mL), and the lowest in children with asthma-exacerbation (median (IQR)=13.982 (7.901-21.624) ng/mL) (P<0.001). At the same time, DUSP1 was also related to decreased asthma risk with area under curve (AUC) (95%CI) of 0.847 (0.780-0.914), and correlated with its lower exacerbation risk with AUC (95%CI) of 0.755 (0.661-0.849). Besides, DUSP1 was negatively linked with exacerbation severity (rs =-0.338, P=0.014), immunoglobulin E (rs =-0.277, P=0.047), TNF-α (rs =-0.423, P=0.002), IL-1ß (rs =-0.389, P=0.004), and IL-17 (rs =-0.293, P=0.035), but not related with other disease features in children with asthma-exacerbation. Meanwhile, DUSP1 was only negatively associated with TNF-α (rs=-0.300, P=0.034) and IL-1ß (rs =-0.309, P=0.029) in children in asthma-remission. However, no correlation was found in DUSP1 with inflammatory cytokines or other disease features in healthy children (all P>0.05). CONCLUSION: DUSP1 reflects the reduced exacerbation risk, and associates with lower exacerbation severity and inflammatory cytokines in children with asthma-exacerbation; it also associates with inflammatory cytokines in children in asthma-remission. These findings suggest that DUSP1 may help to improve the management of asthmatic children.

Therapeutic effect of the sulforaphane derivative JY4 on ulcerative colitis through the NF-κB-p65 pathway.

The efficacy of the sulforaphane derivative JY4 was evaluated in acute and chronic mouse models of ulcerative colitis induced by dextran sodium sulfate. Oral administration of JY4 led to significant improvements in symptoms, with recovery of body weight and colorectal length, together with reduced diarrhoea, bloody stools, ulceration of colonic tissue and infiltration of inflammatory cells. The oral bioavailability of JY4, determined by comparing oral dosing with injection into the tail vein, was 5.67%, which was comply with the idea in the intestinal function. Using a dual-luciferase reporter assay, immunofluorescence studies, western blot analysis and immunohistochemical staining, JY4 was shown to significant interfere with the NF-κB-p65 signaling pathway. By preventing the activation of NF-κB-p65, JY4 inhibited the overexpression of downstream inflammatory factors, thereby exerting an anti-inflammatory effect on the intestinal tract. This study thus provides a promising candidate drug, and a new concept for the treatment of ulcerative colitis.

The Protective Effects of Helicobacter pylori Infection on Allergic Asthma.

As an ancient Gram-negative bacterium, Helicobacter pylori has settled in human stomach. Eradicating H. pylori increases the morbidities of asthma and other allergic diseases. Therefore, H. pylori might play a protective role against asthma. The "disappearing microbiota" hypothesis suggests that the absence of certain types of the ancestral microbiota could change the development of immunology, metabolism, and cognitive ability in our early life, contributing to the development of some diseases. And the Hygiene Hypothesis links early environmental and microbial exposure to the prevalence of atopic allergies and asthma. Exposure to the environment and microbes can influence the growing immune system and protect subsequent immune-mediated diseases. H. pylori can inhibit allergic asthma by regulating the ratio of helper T cells 1/2 (Th1/Th2), Th17/regulatory T cells (Tregs), etc. H. pylori can also target dendritic cells to promote immune tolerance and enhance the protective effect on allergic asthma, and this effect relies on highly suppressed Tregs. The remote regulation of lung immune function by H. pylori is consistent with the gut-lung axis theory. Perhaps, H. pylori also protects against asthma by altering levels of stomach hormones, affecting the autonomic nervous system and lowering the expression of heat shock protein 70. Therapeutic products from H. pylori may be used to prevent and treat asthma. This paper reviews the possible protective influence of H. pylori on allergic asthma and the possible application of H. pylori in treating asthma.

Bifidobacterium plays a protective role in TNF-α-induced inflammatory response in Caco-2 cell through NF-κB and p38MAPK pathways.

Kawasaki disease is an immune-mediated acute, systemic vasculitis and is the leading cause of acquired heart disease in children in the developed world. Bifidobacterium (BIF) is one of the dominant bacteria in the intestines of humans and many mammals and is able to adjust the intestinal flora disorder. The Caco-2 cell monolayers were treated with tumor necrosis factor-α (TNF-α) at 10 ng/ml for 24 h to induce the destruction of intestinal mucosal barrier system. Cells viability was detected through Cell Counting Kit-8 assay. Cell apoptosis was measured by flow cytometry and the expression of apoptosis related proteins was also detected through Western blot. The level of pro-inflammatory cytokines interleukin-6 (IL-6) and IL-8 was detected through ELISA, Western blot and qRT-PCR, respectively. Transepithelial electrical resistance (TEER) assay was conducted to value the barrier function of intestinal mucosa. Cell autophagy and NF-κB and p38MAPK pathways associated proteins were examined through Western blot. In the absence of TNF-α treatment, cell viability and apoptosis showed no significant change. TNF-α decreased cell viability and increased cell apoptosis and BIF treatment mitigated the TNF-α-induced change. Then, we found that BIF treatment effectively suppressed TNF-α-induced overexpression of IL-6 and IL-8. Besides, the results of TEER assay showed that barrier function of intestinal mucosa which was destroyed by TNF-α was effectively recovered by BIF treatment. In addition, TNF-α induced autophagy was also suppressed by BIF. Moreover, TNF-α activated NF-κB and p38MAPK signal pathways were also blocked by BIF, SN50 and SB203580. Our present study reveals that BIF plays a protective role in TNF-α-induced inflammatory response in Caco-2 cells through NF-κB and p38MAPK pathways.

Design and synthesis of novel dasatinib derivatives as inhibitors of leukemia stem cells.

We used the concept of bioisosteres to design and synthesize a novel series of dasatinib derivatives for the treatment of leukemia. Unfortunately, most of the dasatinib derivatives did not show appreciable inhibition against leukemia cell lines K562 and HL60. However, acrylamide compound 2c had comparable inhibitory activity with dasatinib against K562 cells (IC50 = 0.039 nM vs. 0.069 nM). And amide compound 2a and acrylamide compound 2c also had comparable inhibitory activity with dasatinib against the leukemia cell line HL60 (IC50 = 0.25 nM and 0.26 nM vs. 0.11 nM). Against the leukemia progenitor cell line KG1a, triazole compounds 15a and 15d-15f and oxadiazole compounds 24a-24d were more potent than dasatinib. In particular, the hydroxyl compounds 15a and 24a were about 64 and 180 fold more potent than dasatinib against KG1a cells (IC50 = 0.14 µM and 0.05 µM vs. 8.98 µM). Compounds 15a and 24a also inhibited colony formation in MCF-7 cells and inhibited cell migration in the cell wound scratch assay in B16BL6 cells. Moreover, hydroxyl compounds 15a and 24a had low toxicity in vivo.

Therapeutic effects of isothiocyanate prodrugs on rheumatoid arthritis.

Isothiocyanates 7a and 7b have poor stability and aqueous solubility. To address these problems, prodrugs 8a and 8b were synthesized. Prodrugs 8a and 8b were stable in HEPES buffer at pH 4.4, but released the active compounds 7a and 7b in HEPES buffer at pH 7.4 and in mouse plasma, respectively. Compound 8a and especially compound 8b showed anti-inflammatory effects. Compound 8b demonstrated significant efficacy in animal models of traumatic inflammation, acute inflammation and rheumatoid arthritis. Compound 8b also did not cause appreciable toxicity in mice after 5 weeks at a daily dose of 200 mg/kg.

Syntheses and biological evaluation of 1,2,3-triazole and 1,3,4-oxadiazole derivatives of imatinib.

Three novel series of 1,2,3-triazole and 1,3,4-oxadiazole derivatives of imatinib were prepared and evaluated in vitro for their cytostatic effects against a human chronic myeloid leukemia (K562), acute myeloid leukemia (HL60), and human leukemia stem-like cell line (KG1a). The structure-activity relationship was analyzed by determining the inhibitory rate of each imatinib analog. Benzene and piperazine rings were necessary groups in these compounds for maintaining inhibitory activities against the K562 and HL60 cell lines. Introducing a trifluoromethyl group significantly enhanced the potency of the compounds against these two cell lines. Surprisingly, some compounds showed significant inhibitory activities against KG1a cells without inhibiting common leukemia cell lines (K562 and HL60). These findings suggest that these compounds are able to inhibit leukemia stem-like cells.

Sulforaphane Analogues with Heterocyclic Moieties: Syntheses and Inhibitory Activities against Cancer Cell Lines.

Recent studies have shown that sulforaphane (SFN) selectively inhibits the growth of ALDH⁺ breast cancer stem-like cells.Herein, a series of SFN analogues were synthesized and evaluated against breast cancer cell lines MCF-7 and SUM-159, and the leukemia stem cell-like cell line KG-1a. These SFN analogues were characterized by the replacement of the methyl group with heterocyclic moieties, and the replacement of the sulfoxide group with sulfide or sulfone. A growth inhibitory assay indicated that the tetrazole analogs 3d, 8d and 9d were significantly more potent than SFN against the three cancer cell lines. Compound 14c, the water soluble derivative of tetrazole sulfide 3d, demonstrated higher potency against KG-1a cell line than 3d. SFN, 3d and 14c significantly induced the activation of caspase-3, and reduced the ALDH⁺ subpopulation in the SUM159 cell line, while the marketed drug doxrubicin(DOX) increased the ALDH⁺ subpopulation.

Asymmetric Synthesis of 1,3-Oxazolidine Derivatives with Multi-Component Reaction and Research of Kinetic Resolution.

An efficient multi-component reaction to synthesize multi-substituted 1,3-oxazolidine compounds of high optical purity was described. All the products were well-characterized and the absolute configuration of one chiral center was determined. The plausible mechanism was proposed and a kinetic resolution of epoxides process was confirmed.

Diagnostic and Predictive Value of LncRNA MCM3AP-AS1 in Sepsis and Its Regulatory Role in Sepsis-Induced Myocardial Dysfunction.

The present study focused on exploring the clinical value and molecular mechanism of LncRNA MCM3AP antisense RNA 1 (MCM3AP-AS1) in sepsis and sepsis-induced myocardial dysfunction (SIMD). 122 sepsis patients and 90 healthy were included. Sepsis patients were categorized into SIMD and non-MD. The expression levels of MCM3AP-AS1 and miRNA were examined using RT-qPCR. Diagnostic value of MCM3AP-AS1 in sepsis assessed by ROC curves. Logistic regression to explore risk factors influencing the occurrence of SIMD. Cardiomyocytes were induced by LPS to construct cell models in vitro. CCK-8, flow cytometry, and ELISA to analyze cell viability, apoptosis, and inflammation levels. Serum MCM3AP-AS1 was upregulated in patients with sepsis. The sensitivity and specificity of MCM3AP-AS1 were 75.41% and 93.33%, for recognizing sepsis from healthy controls. Additionally, elevated MCM3AP-AS1 is a risk factor for SIMD and can predict SIMD development. Compared with the LPS-induced cardiomyocytes, inhibition of MCM3AP-AS1 significantly attenuated LPS-induced apoptosis and inflammation; however, this attenuation was partially reversed by lowered miR-28-5p, but this reversal was partially eliminated by CASP2. MCM3AP-AS1 may be a novel diagnostic biomarker for sepsis and can predict the development of SIMD. MCM3AP-AS1 probably participated in SIMD progression by regulating cardiomyocyte inflammation and apoptosis through the target miR-28-5p/CASP2 axis.

A review on micro- and nanoplastics in humans: Implication for their translocation of barriers and potential health effects.

As emerging contaminants, micro- and nanoplastics (MNPs) can absorb and leach various toxic chemicals and ultimately endanger the health of the ecological environment and humans. With extensive research on MNPs, knowledge about MNPs in humans, especially their translocation of barriers and potential health effects, is of utmost importance. In this review, we collected literature published from 2000 to 2023, focusing on MNPs on their occurrence in humans, penetrating characteristics in the placental, blood-brain, and blood-testis barriers, and exposure effects on mammalian health. The characteristics and distributions of MNPs in human samples were analyzed, and the results demonstrated that MNPs were ubiquitous in most human samples, except for kidneys and cerebrospinal fluid. In addition, the phenomenon of MNPs crossing barriers and their underlying mechanisms were discussed. We also summarized the potential factors that may affect the barrier crossing and health effects of MNPs, including characteristics of MNPs, exposure doses, administration routes, exposure durations, co-exposure to other pollutants, and genetic predisposition. Exposure to MNPs may cause cytotoxicity, neurotoxicity, and developmental and reproductive toxicity in mammals. People are encouraged to reduce their exposure to MNPs to prevent these adverse health effects. Finally, we discussed the shortcomings of current research on MNPs in humans, providing a valuable reference for understanding and evaluating the potential health risks from MNP exposure in mammals, including humans.

Eosinophilic granulomatous polyangiitis with central nervous system involvement in children: a case report and literature review.

Objective: To explore the clinical characteristics and treatment outcomes of children with central nervous system (CNS) involvement in eosinophilic granulomatosis with polyangiitis (EGPA). Methods: A child who presented with EGPA complicated by CNS involvement was admitted to our hospital in June 2023. The clinical features were analyzed retrospectively, and relevant literatures were reviewed to provide a comprehensive overview of this condition. Results: A ten-year-old girl, who had a history of recurrent cough and asthma accompanied by peripheral blood eosinophilia for eight months, was admitted to our hospital. On admission, spotted papules were visible on her hands and feet, bilateral pulmonary rales were audible. The laboratory examination revealed that the proportion of eosinophils (EOS) exceeded 10% of white blood cells, the anti-neutrophil cytoplasmic antibody (MPO-ANCA) was positive, the immunoglobulin G level was 15.80g/L, and the immunoglobulin E level was greater than 2500.00IU/mL. The imaging examination showed multiple patchy and nodular high-density shadows in both lungs as well as sinusitis. Pulmonary function tests indicated moderate ventilation and diffusion dysfunction. Bone marrow cytology demonstrated a significant increase in the proportion of eosinophils. Skin pathology confirmed leukocytoclastic vasculitis. During the hospitalization, the child had a convulsion. The magnetic resonance imaging (MRI) scan of the brain showed multiple abnormal signal shadows in the bilateral cerebral cortex and the electroencephalogram (EEG) showed epileptic waves. Following the administration of methylprednisolone pulse therapy in combination with cyclophosphamide treatment, her cough and asthma resolved, the skin rash disappeared without any further convulsions. We found that only a young EGPA patient with CNS involvement had been previously reported. The previously reported case began with long-term fever, weight loss, and purpuric rash. Both patients responded well to treatment with glucocorticoids and cyclophosphamide, experiencing significant improvement in their clinical symptoms and normalization of their peripheral blood eosinophils. Conclusion: The diagnosis of EGPA in children can be challenging. When a child is affected by EGPA, it is essential to remain vigilant for signs of CNS involvement. The treatment with glucocorticoids and cyclophosphamide is effective in managing EGPA in children.

Analyzing the impact of ambient temperature indicators on transformer life in different regions of Chinese mainland.

Regression analysis is applied to quantitatively analyze the impact of different ambient temperature characteristics on the transformer life at different locations of Chinese mainland. 200 typical locations in Chinese mainland are selected for the study. They are specially divided into six regions so that the subsequent analysis can be done in a regional context. For each region, the local historical ambient temperature and load data are provided as inputs variables of the life consumption model in IEEE Std. C57.91-1995 to estimate the transformer life at every location. Five ambient temperature indicators related to the transformer life are involved into the partial least squares regression to describe their impact on the transformer life. According to a contribution measurement criterion of partial least squares regression, three indicators are conclusively found to be the most important factors influencing the transformer life, and an explicit expression is provided to describe the relationship between the indicators and the transformer life for every region. The analysis result is applicable to the area where the temperature characteristics are similar to Chinese mainland, and the expressions obtained can be applied to the other locations that are not included in this paper if these three indicators are known.

Downregulation of miR-17~92 Expression Increase Paclitaxel Sensitivity in Human Ovarian Carcinoma SKOV3-TR30 Cells via BIM Instead of PTEN.

To better understand the molecular mechanisms of paclitaxel resistance in ovarian carcinoma, we evaluated the expression of miRNAs using miRNA microarray between human ovarian carcinoma SKOV3 cells and paclitaxel resistant SKOV3-TR30 cells. Results showed that 69 miRNAs were upregulated while 102 miRNAs were downregulated in SKOV3-TR30 cells. Using real-time PCR, we further clarified that miR-17~92 was overexpressed in SKOV3-TR30 cells compared with that in SKOV3 cells. We then established stable virally transduced SKOV3-TR30-m-PTIP-Sponge all SKOV3-TR30 cells and its vector-only control SKOV3-TR30-m-PTIP-GFP cells. Real time-PCR revealed that SKOV3-TR30-m-PTIP-Sponge all cells expressed approximately 6.18-fold lower levels of miR-17~92 compared with the control group. Decreased expression of miR-17~92 resulted in cell cycle arrest in the G2/M phase and growth inhibition. After the transduction, the BIM protein level was increased in SKOV3-TR30 cells and luciferase reporter assays revealed that miR-17~92 binds directly to the 3'-UTR of BIM. Results of luciferase reporter assays accompanied with Western Blot showed that although miR-17~92 binds directly to the 3'-UTR of PTEN, the PTEN protein expression level was upregulated slightly while the result is of no statistical significance. Our results showed that miR-17~92 could be a causal factor of the downregulation of BIM in SKOV3-TR30 cells and thus induce the paclitaxel resistance in SKOV3-TR30 cells.

An EGSB-SBR based process for coupling methanogenesis and shortcut nitrogen removal.

An integrated process consisting of an anaerobic/anoxic expanded granular sludge bed (EGSB) reactor and an aerobic sequencing batch reactor (SBR) was developed by a mode of sequencing batch operation, in which methanogenesis, denitrification and anammox were coupled in EGSB with methanogenesis first, then denitrification and anammox simultaneously, and partial nitrification occurred in SBR for providing nitrite to EGSB. This process extended the application of the anammox process to the treatment of wastewater containing high concentrations of chemical oxygen demand (COD) and ammonium. When the volumetric exchange ratio between EGSB and SBR was controlled at 57% with the influent pH at 6-8, 74.38-83.65% of NH(4)(+)-N, 72.68-83.12% of total nitrogen (TN) and 88.34-98.86% of COD were removed in a range of 200-4,500 mg/L COD and 40-90 mg/L NH(4)(+)-N respectively. TN removal by anammox and shortcut denitrification was 26.35-58.64 and 0-32.80% of the removed nitrogen, respectively. The results showed that the contribution of anammox gradually decreased with an increase in the C/N ratio of influent, whereas the reverse was true for shortcut denitrification. The COD removal by methanogenesis was 70.89-98.79% of the removed COD, and increased with increasing C/N ratio.

A rapid method for extracting microplastics from oily food samples.

The increasing evidence of microplastic (MP) contamination influence on aquatic organisms has been extensively reported globally. However, the discussions of extracting MPs from oily food samples are limited, highlighting the pressing need for effective and standardized analytical methods to extract MPs from oily food. Previous methods, such as using acid, alkali or oxidizing solutions as digestion reagents, usually take a long time to digest oily food, increasing the possibility of procedural contamination of MPs in food over time. The objective of this study was to develop a rapid, efficient, economical and simple analytical method to extract MPs from oily food samples. This innovative protocol combines the use of 4 : 1 HNO3 : H2O2 as a digestion reagent to accelerate the digestion within 1 h at 50 °C and hexane as a washing solution to remove the oil adsorbed on the surface of MPs and membranes. Four common types of MPs, namely, polyethylene terephthalate, polyethylene, polystyrene and polypropylene of different sizes were added to oily flours to demonstrate this method. The mean recovery of MPs was 95% ± 2% (range: 93-98%), and no significant changes in color, particle size, surface area and spectrum features were found for all recovered polymers except for PS with minor changes in color and surface. The method was confirmed to be effective on rice, noodles, bean products and various meat samples. All in all, the present method can facilitate the observation and identification of characteristics of MPs, providing an innovative combination method for quantitative and qualitative analyses of MPs in oily food samples.